In this episode, I introduce a diagnosis that is not a diagnosis. By that, I mean that it is a condition that we may find our patients in, but it is not considered to be a diagnosis by itself, like major depressive disorder or schizophrenia are considered to be diagnoses. I am talking about catatonia, a condition characterized by either a lack of interaction with the world or as purposeless interaction with the world.
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Welcome to PsyDactic - Residency Edition - Your podcast resource to survive and thrive in your psych residency.
I am Dr. O, and as of this recording I am a 2nd Year Resident in the National Capital Consortium Psychiatry Residency Program. However, make no mistake, I do not speak for this program, nor do I speak for the Department of Defense or the Federal Government or anyone else for that matter. What I say is my opinion, and I reserve the right to be wrong, so trust me at your own risk. It’s a risk some are willing to take.
References and recommended readings can be found at the end of the show transcript, located at psydactic.buzzsprout.com.
Before I get started here, I want to take another chance to turn you on to another resource out there for psych residents and med studs. It’s called bullet psych located at www.bulletpsych.com, and it gives you the option of signing up for a free daily email stream of content in bite sized chunks to learn about psychiatric disorders. It’s created by a fellow residency colleague of mine, Dr. Marcus Hunt, and for those of you, like me, who tend to fall asleep after reading about 3 paragraphs, it may be just the thing for you. It is concise, well-organized, and somehow still manages to give a good thorough treatment of its subject. So try googling bullet psych and see where it takes you. By the way, Dr. Hunt is not paying me to say this, I do it of my own free will and admiration.
Today I want to talk about a diagnosis that is not a diagnosis. By that, I mean that it is a condition that we may find our patients in, but it is not considered to be a diagnosis by itself, like major depressive disorder or schizophrenia are considered to be diagnoses. I am talking about catatonia, a condition characterized by either a lack of interaction with the world or as purposeless interaction with the world. It has been called Kahlbaum Syndrome after its first describer, German Psychiatrist Karl Ludwig Kahlbaum. It appears that Kahlbaum conceptualized catatonia as its own entity, but others disagreed. Emil Wilhelm Georg Magnus Kraepelin, another German Psychiatrist, racist and eugenicist, argued that catatonia was simply a manifestation of schizophrenia or dementia praecox as he called it. Since this time, catatonia has been found to be more common in mood disorders than in schizophrenia, and can be seen in some sense as an acute and potentially chronic brain failure with its own distinct features.
You’ll find the diagnostic criteria for catatonia in the Schizophrenia Spectrum and Other Psychotic Disorders chapter in the DSM 5, which seems to represent more of an historical nod to Kraepelin than to careful categorization. In the DSM, this condition continues to be considered a specifier for other conditions such as schizophrenia or mood disorders or it can be diagnosed as secondary to a medical condition. If you don’t know what caused it, you can label it Unspecified Catatonia. Other than the Unspecified designation, you can’t simply diagnose a patient with catatonia. You have to figure out what is causing the catatonia and diagnose that. This is important, because although catatonia has its own treatment course and prognosis, if you don’t treat the underlying condition that resulted in catatonia, you haven’t fully treated catatonia.
But, “What,” you might ask, “is catatonia?” The DSM 5 states you have to have 3 features from a list of 12 diagnostic signs. From what I have read, it seems that using the cut-off of 3 symptoms is both highly specific and sensitive, but there is no real gold standard to compare it to. Unlike many diagnoses in the DSM, none of the features of catatonia are subjective symptoms (at least not subjective to the patient report). They are signs that you should be able to identify in a patient. For the sake of time in this episode, I am going to list the signs and give brief descriptions. In later episodes, I will explore the pathophysiology and particular definitions of these signs in more detail.
The 12 signs of catatonia in the DSM 5 are these:
So there you have it, the 12 disciples of catatonia. Some of these seem very related, like echolalia and echopraxia, or catalepsy, postering and grimacing, or stupor and mutism, or mannerisms and stereotypy. However, it does not matter which of the 3 you find, it remains catatonia.
I want to reiterate here that I am not going to go into deep discussion of these signs here. I will do that in the future when I talk about the causes of catatonia. For now, I am going to go onto what you need to do when you see these things. First, you need to make sure you are not confusing catatonia with something else, like delirium. Second, you need to immediately treat the catatonia. Third, you need to treat the underlying cause.
So let's get started.
First, don’t confuse catatonia with something else. Catatonia comes in a few different flavors. In the English literature, it is most often distinguished by two different presentations called “retarded or excited.” I have also seen it called “akinetic and hyperkinetic.” Retarded or akinetic presentation are predominated by the signs that lack movement or response, such as stupor, catalepsy, mutism, and negativism. Excited or hyperkinetic catatonia is identified by the movement-unrestricted signs such as agitation, stereotypy, and mannerisms. By far, the most commonly reported presentation of catatonia is the retared or akinetic type. What is most worrisome about catatonia is the potential for it to progress to malignant catatonia which is very similar to neuroleptic malignant syndrome. There is a pathological increase in muscle tone leading to rhabdomyolysis, kidney failure, seizures, arrhythmias and death.
There are a number of other psychiatric disorders that you don’t want to confuse with catatonia. I think the most obvious culprit is delirium, which also comes in two distinct varieties, which are termed hyperactive and hypoactive. However, in delirium patients often have perceptual disturbances, have variable levels of orientation to their surroundings, and lack the ability to maintain their attention. This is quite often associated with procedural sedation, metabolic abnormalities, toxic ingestion, infections or systemic inflammation. Delirious patients may be seen to be staring forward, but you can redirect their gaze. They may be agitated, but unlike in catatonia, they can articulate a purpose, like they want the staff to leave them alone, they want to leave the hospital, or they are hallucinating words written all over the walls of their room. They may be minimally interactive, but this changes throughout the day, and is not associated with an increase in muscle tone or posturing. Also, patients with delirium often show diffuse slowing on EEG. Catatonic patients may also have diffuse slowing on EEG, but they are frequently normal. In this case, EEG is unlikely to make a good tie breaker.
There are some conditions in which patients are minimally interactive or mute. Abulia is a condition in which a patient is fully aware and has no cognitive or motor disturbances, but is apathetic and unmotivated. In its extreme form, apathy results in a condition called akinetic mutism. These patients also won’t have any of the “tonia” that catatonic patients have, nor will they demonstrate the unrestrained motor activity of excited catatonia. If you are unsure if your patient is catatonic or experiencing akinetic mutism, you can do an “Ativan challenge,” and see if a little lorazepam improves their condition.
Other things not to be confused with catatonia are extrapyramidal symptoms secondary to antipsychotic use. Antipsychotics can cause an increase in muscle tone and abnormal movements due to its effects on the striatum. They can also contribute to or mimic the negative symptoms of schizophrenia. What is great about EPS and catatonia is if you are not sure which it is, that doesn’t make a huge difference in how you would treat the patient. If you are not sure whether they have EPS or catatonia, you should stop antipsychotics and give some lorazepam, because this is helpful in both conditions and can help prevent progression to neuroleptic malignant syndrome or malignant catatonia.
Other conditions that might mimic catatonia include certain forms of epilepsy, locked-in syndrome, or even a vegetative state. A good patient history along with EEG and/or MRI may help distinguish these etiologies which may resemble akinetic or retarded catatonia.
After ruling out other conditions that look similar to catatonia, you can treat. It is important to not give antipsychotics to patients with catatonia, even if they have schizophrenia because it predisposes them to neuroleptic malignant syndrome. Instead, give benzos. Give 1MG of Ativan, and if that doesn’t work, give 2MG of Ativan, and if that doesn’t work, give 3MG Ativan, and if that doesn’t work, give more Ativan. Small and old patients may need less Ativan. If you start with a very low dose, then it is reasonable to give another dose after 30 minutes if there is no response. If your dose is higher than 1MG, then you may want to wait about 3 hours between doses. Around 80-90% of patients with catatonia have a good response to lorazepam, which is seen as a return to relatively normal motor functioning. The akinetic patient will become interactive and the hyperkinetic patient will calm down. For some reason though, only 50-60% of schizophrenic patients with catatonia will have such robust responses.
You can often treat catatonia empirically, even if you are not sure if it is actually catatonia, because the treatment is unlikely to harm a patient, though giving benzos to a patient with delirium may result in disinhibition. If lorazepam doesn’t work and ECT is available, give them a few rounds of ECT. This is also highly effective and for malignant catatonia, you should not hesitate to give ECT as soon as possible if the patient is not immediately responding to pharmacologic treatments.
There are a number of other much less effective treatment options. For some patients, an excess of glutamatergic tone may be contributing to catatonia, so trying memantine or amantadine (both glutamate blockers) is reasonable. Instead of increasing inhibitory tone in the brain, these drugs would decrease the excitatory tone. It is unclear how effective they actually are, but in patients where catatonia is caused by NMDA encephalitis, it is reasonable to target the NMDA receptor itself. Other drugs that potentiate GABA such as the z-drugs like zolpidem are also reasonable choices or could be used in the maintenance phase of treatment, which may be necessary to prevent relapse into catatonia.
The final thing I want to leave you with in this episode is TREAT THE UNDERLYING CAUSE. Catatonia is a movement disorder which is most often the result of some other underlying disorder. Catatonia is more common in mood disorders than in psychotic disorders. Treating the underlying depression or bipolar or psychosis is key. One of the difficulties can be that patients with catatonia should not be on antipsychotics with a moderate to high potential for EPS because this results in higher rates of progression to NMS or malignant catatonia. Various other neurological and medical disorders can also result in catatonia including some strokes, autoimmune disorders, and CNS infections. If you don’t treat these conditions, the catatonia is unlikely to improve or is more likely to relapse.
I have wanted to talk about catatonia for a long time. In future episodes, I will go into more detail about proposed neurobiology and pathophysiology of catatonia as well as how to clearly understand and identify the signs of catatonia. Once you learn about catatonia, you’ll start to see signs of it everywhere, and it is important to know whether this is a true sign or a mimic.
I am Dr. O, and this has been an episode of PsyDactic - Residency Edition. 1–3
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2. Ellul P, Choucha W. Neurobiological approach of catatonia and treatment perspectives. Front Psychiatry. 2015;6:182. doi:10.3389/fpsyt.2015.00182
3. Kaufmann C, Agalawatta N, Malhi GS. Catatonia: Stereotypies, mannerisms and perseverations. Aust N Z J Psychiatry. 2018;52(4):391-393. doi:10.1177/0004867418765669